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http://purl.uniprot.org/citations/26892022http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/26892022http://www.w3.org/2000/01/rdf-schema#comment"Different modes of cell death regulate immunity. Whereas necrotic (necroptotic, pyroptotic) cell death triggers inflammation, apoptosis contributes to its resolution. Interleukin-1 (IL-1) family cytokines are key players in this interaction. A number of IL-1 family cytokines are produced by necrotic cells to induce sterile inflammation. However, release of IL-1 family proteins from apoptotic cells to regulate inflammation was not described. Here we show that IL-38, a poorly characterized IL-1 family cytokine, is produced selectively by human apoptotic cells to limit inflammation. Depletion of IL-38 in apoptotic cells provoked enhanced IL-6 and IL-8 levels and AP1 activation in co-cultured human primary macrophages, subsequently inducing Th17 cell expansion at the expense of IL-10-producing T cells. IL-38 was N-terminally processed in apoptotic cells to generate a mature cytokine with distinct properties. Both full-length and truncated IL-38 bound to X-linked interleukin-1 receptor accessory protein-like 1 (IL1RAPL1). However, whereas the IL-38 precursor induced an increase in IL-6 production by human macrophages, truncated IL-38 reduced IL-6 production by attenuating the JNK/AP1 pathway downstream of IL1RAPL1. In conclusion, we identified a mechanism of apoptotic cell-dependent immune regulation requiring IL-38 processing and secretion, which might be relevant in resolution of inflammation, autoimmunity, and cancer."xsd:string
http://purl.uniprot.org/citations/26892022http://purl.org/dc/terms/identifier"doi:10.1093/jmcb/mjw006"xsd:string
http://purl.uniprot.org/citations/26892022http://purl.uniprot.org/core/author"Han Y."xsd:string
http://purl.uniprot.org/citations/26892022http://purl.uniprot.org/core/author"Frank A.C."xsd:string
http://purl.uniprot.org/citations/26892022http://purl.uniprot.org/core/author"Jung M."xsd:string
http://purl.uniprot.org/citations/26892022http://purl.uniprot.org/core/author"Mora J."xsd:string
http://purl.uniprot.org/citations/26892022http://purl.uniprot.org/core/author"Wittig I."xsd:string
http://purl.uniprot.org/citations/26892022http://purl.uniprot.org/core/author"Richter F."xsd:string
http://purl.uniprot.org/citations/26892022http://purl.uniprot.org/core/author"Ernst A."xsd:string
http://purl.uniprot.org/citations/26892022http://purl.uniprot.org/core/author"Weigert A."xsd:string
http://purl.uniprot.org/citations/26892022http://purl.uniprot.org/core/author"Brune B."xsd:string
http://purl.uniprot.org/citations/26892022http://purl.uniprot.org/core/author"Putyrski M."xsd:string
http://purl.uniprot.org/citations/26892022http://purl.uniprot.org/core/author"Schlemmer A."xsd:string
http://purl.uniprot.org/citations/26892022http://purl.uniprot.org/core/date"2016"xsd:gYear
http://purl.uniprot.org/citations/26892022http://purl.uniprot.org/core/name"J Mol Cell Biol"xsd:string
http://purl.uniprot.org/citations/26892022http://purl.uniprot.org/core/pages"426-438"xsd:string
http://purl.uniprot.org/citations/26892022http://purl.uniprot.org/core/title"Interleukin-38 is released from apoptotic cells to limit inflammatory macrophage responses."xsd:string
http://purl.uniprot.org/citations/26892022http://purl.uniprot.org/core/volume"8"xsd:string
http://purl.uniprot.org/citations/26892022http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/26892022
http://purl.uniprot.org/citations/26892022http://xmlns.com/foaf/0.1/primaryTopicOfhttps://pubmed.ncbi.nlm.nih.gov/26892022
http://purl.uniprot.org/uniprot/#_P45983-mappedCitation-26892022http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/26892022
http://purl.uniprot.org/uniprot/#_Q8WWZ1-mappedCitation-26892022http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/26892022
http://purl.uniprot.org/uniprot/#_Q9NZN1-mappedCitation-26892022http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/26892022
http://purl.uniprot.org/uniprot/#_Q9HB29-mappedCitation-26892022http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/26892022